Midterm 2 flash cards

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1
Q

What are the methods of control of the immune system

A

-cytokines signaling proteins amplifying/supressing
-Tolerance so immune system dosent attack itself
-Regulatory (tregs) which are peackeers preventing overreation
-Activation/Apoptosis balance

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2
Q

Ways that the immune system are shut off

A

Indirectly:less antigen present to stimulate an immune response so DCs die after a few days

Directly:Apoptosis and by molecular inhibition of immune functions (activated T cells are inherently pro apoptotic

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3
Q

Molecular examples of Direct immune response

A

Tim-3:A receptor on T cells that inhibits their activation and promotes cell death
PD1/ PD1L: PD-1 on T cells binds to PD-L1 to suppress immune responses, helping tumors evade detection
CTLA-4:receptor competes with CD28 to inhibit T cell activation, promoting immune tolerance.

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4
Q

IL-2 is for what?

A

-Produced by T cells and is the main growth factor for T cells.
-When T cell activated, they produce IL-2 leading to cell division and immune cell expansion.

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5
Q

IL-4 is for what?

A

-made by macrophages and Th2 cells
-Help naïve Th cells (immature T helper cells) develop into Th2 cells.
-Stimulate the immune system to produce antibodies.

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6
Q

IL-5

A

produced by Th2 cells and it functions to promote the growth and
differentiation of B cells and eosinophils. It also activates mature eosinophils.

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7
Q

TGF-β

A

It inhibits the proliferation of T cells and the activation of macrophages

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8
Q

INF-γ

A
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9
Q

What are the different pathogens each adaptive system is more geared to?

A

Th1: viral/bacterial attacks in the blood and tissue
Th2: mucosal/parasitic infections.

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10
Q

central tolerance says that

A

-B and T cells must:
not react to self antigens
-Be restricted to self MHC molecules (T cells), so they will only react to presented antigens

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11
Q

Where is cell selection done

A

epithelial cells in the cortex

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12
Q

positive selection is when?

A

Cells that recognize MHC-peptide
complexes receive rescue signals that
Prevent apoptosis.

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13
Q

What happens to CD4 and CD8 T cells that survive MHC

A

migrate to the medulla of the thymus where they are
Tested for response to self antigens

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14
Q

Negative selection is a process that happens in… and prevent…

A

Negative selection is a process that happens in the thymus to prevent T cells from attacking the body’s own tissues.

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15
Q

explain how negative selection happens:

A

1)Thymic dendritic cells show T cells samples of self-peptides using MHC molecules.

2)The AIRE gene helps thymic cells produce proteins from various organs, even though those proteins are normally only found in specific parts of the body. This gives T cells a wide view of what “self” looks like.

3)The dendritic cells essentially present a “snapshot” of self-proteins from around the body to the developing T cells.

4)If a T cell binds too strongly to these self-peptides presented by MHC, it is seen as a threat because it might attack the body’s own cells. As a result, the T cell is deleted (undergoes apoptosis), preventing autoimmunity.

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16
Q

explain tregs:

A

Regulatory T cells (Tregs) are made in the thymus as part of the immune system’s self-regulation process.

Some CD4 T cells that have a slightly stronger reaction to the body’s own proteins (self-antigens) during negative selection are turned into natural Tregs (nTreg) instead of being eliminated.

About 5% of the CD4 T cells circulating in your body are these natural Tregs.

Unlike helper T cells, which activate the immune response, Tregs suppress or “turn down” the immune response to prevent it from attacking the body’s own cells.

In addition to natural Tregs, inducible (adaptive) Tregs can develop later in response to inflammation, and they can help regulate the immune response to both self and foreign antigens after an immune reaction.

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17
Q

what does maintaining peripheral tolerance mean

A

prevent the immune system from attacking the body’s own tissues.

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18
Q

What do treg cells produce that help calm the immune system down

A

anti-inflammatory cytokines like IL-10 and TGF-β

19
Q

Name two main things treg cells do

A

-regulate activation of other T cells
-maintain peripheral tolerance to self antigens
-Produce cytokines that shut down the immune system

20
Q

What tests do B cells undergo

A

1) postitive selection: make sure BCR receptors are working
2) Negative selection: make sure cells dont react to self.

21
Q

Difference between B and T cell growth in terms of which is easier to make

A

60 mil T cells are made & ONLY 2 million make it
meanwhile
30-40% B cells survive

22
Q

What does compartmentalization mean

A

Naive t cells don’t get exposed to everything that could trigger an immune response. becuase they are floating around the body and the chance for them to meet one is lower than if it was in the lymph nodes.

23
Q

What is co-stimulation

A

When T cells encounter antigens outside the thymus binds to an antigen through its T-cell receptor if it doesn’t get a second “go-ahead” signal from innate immune cells the T cell either:
Becomes inactive (this is called anergy), or
Undergoes programmed cell death (apoptosis).

24
Q

How T cells get activated:

A

1) Their T-cell receptor (TCR) must recognize and strongly bind to an MHC/peptide complex (this shows them what to attack).
2)They also need a “go-ahead” signal, called co-stimulation, which usually comes from a protein called CD28 on the T cell binding to B7 molecules
(At first, T cells have a lot of CD28 on their surface to help them get that co-stimulation signal.
However, as the T cells keep getting stimulated (encountering the antigen), they start putting a different protein, CTLA-4, on their surface.
CTLA-4 competes with CD28 for the same B7 molecules, but CTLA-4 binds B7 1,000 times better than CD28)
When CTLA-4 binds to B7, it takes away the opportunity for CD28 to get the “go-ahead” signal.
This blocks CD28’s ability to fully activate the T cell. In other words, CTLA-4 slows down or stops the T cell from continuing to attack by reducing the number of B7 molecules available.

25
Q

what causes Hypersensitivity reactions

A

Failure in Tolerance or immune control mechanisms can lead to the development of Hypersensitivity reactions

26
Q

What are the four types of hypersensitivity reactions

A

Type I: Allergy (immediate)
Type II: Cytotoxic
Type III: Immune complex
Type IV: Delayed hypersensitivity or cell-mediated hypersensitivity

27
Q

Explain how Allergies work

A

Sensitization Phase:

The first time a person encounters an allergen like pollen, their immune system responds by producing a specific type of antibody called IgE.
These antibodies attach to special cells in the body called mast cells and basophils. This is known as sensitization—it’s like the immune system is “preparing” for a future attack from that allergen.

Subsequent Exposure:
If the person comes into contact with the same allergen again, the IgE antibodies on the mast cells and basophils recognize it. This triggers these cells to release various chemicals, including histamine.
Histamine and other mediators are responsible for the symptoms associated with allergies.

28
Q

what is the word to describe a rash

A

Uticaria

29
Q

Someone being Atopic means what

A

prone to developing allergic reactions, like asthma, eczema, or hay fever

30
Q

What is Atopic march

A

refers to the typical progression of allergic diseases in these individuals, starting with eczema in early life, followed by food allergies, and eventually asthma or hay fever.

31
Q

what cells are involved in allergic reactions

A

Th2 activate B cells which then produce IgE

32
Q

What cytokeins regulate the immune response in allergies

A

IL-4, IL-5, and TGF-beta

33
Q

what happens in cytotoxic hypersensitivity

A

IgM and IgG mistakingly bind to antigens on the surface of body’s own cells which triggers complement.

34
Q

list examples of type 2 cytotoxic hypersensitivity.

A

1)Autoimmune Hemolytic Anemia: The immune system attacks RBC
2)Blood Transfusion Reactions: If you receive blood of an incompatible type, your immune system can attack the transfused red blood cells, causing them to be destroyed.
3)Rh Hemolytic Disease: This happens when a pregnant woman’s immune system attacks her baby’s red blood cells if there’s an Rh blood type mismatch.
4)Autoimmune Glomerulonephritis: The immune system mistakenly targets the kidneys, leading to inflammation and potential damage to the kidneys.

35
Q

What is type III immune complex in hypersensitivity.

A

the immune system forms complexes made of antibodies and antigens which are not cleared properly and trigger complement. then neutrophils are recrutied to try and clean up the place but it just causes inflammation.

36
Q

list examples of type 3 immune complex hypersensitivity.

A

1) Rheumatoid Arthritis (RA): In RA, immune complexes deposit in the joints, leading to inflammation, pain, and joint damage.
2) Systemic Lupus Erythematosus: In SLE, immune complexes can deposit in various organs like the skin, kidneys, and joints, causing widespread tissue damage.
Some Types of Glomerulonephritis: Immune complexes can lodge in the kidneys, leading to inflammation and kidney damage.

37
Q

What happens type IV delayed hypersensitivity.

A

T lymphocytes are sensitized and activated on second contact with same antigen. Th1 Lymphokines are relased and induce inflammation and activate macrophages and CD8. causes the cell to attack target but also hurt self along the way.

38
Q

List examples of type IV delayed hypersensitivity.

A

1)Contact Dermatitis: A delayed skin reaction after contact with allergens like poison ivy, nickel, or latex. The skin becomes inflamed and itchy.
2)Type 1 Diabetes (Diabetes Mellitus): In this autoimmune disease, T cells attack beta cells which produce insulin the pancreas.
3)Rheumatoid Arthritis: T cells are involved in attacking the joints, leading to inflammation and damage.

39
Q

Autoimmunity can occur when…list 3 reasons

A

1) Individual express MHC molecules that efficiently present self peptides
Two particular types of MHCII increase chance of type1 diabetes by 20 fold

2)The production of T and B cells involves a random process of creating unique receptors, which means there’s always a chance that some cells might accidentally recognize the body’s own tissues as harmful. Even identical twins, despite having the same genetic makeup, will not have exactly the same immune cell receptors because of the randomness in this process.

3)Breakdown of tolerance mechanisms designed to eliminate these cells

40
Q

Break down in immune function/tolerance

A

1)Central tolerance problems: if system fails, these self-reactive immune cells may survive and cause autoimmunity.

2)T Reg cells are special immune cells that help suppress immune responses to the body’s own tissues, maintaining tolerance. If there are problems with the function or number of T Reg cells, it can lead to the immune system attacking healthy tissues.

3) Defective Apoptosis

4)Inhibitory receptors like CTLA-4 normally act as brakes for the immune system, preventing overactivity. If these receptors don’t work properly, the immune response can go into overdrive, causing damage to the body.

5) Chronic Activation of Immune Cells:
Antigen-presenting cells (APCs), which show immune cells what to attack, and T cells can become overly active, leading to continuous immune responses even when they aren’t needed. This can cause chronic inflammation and damage.

41
Q

What happens in Molecular Mimicry

A

Autoimmune diseases can occur when TCRs or BCRs, which are generated randomly, mistakenly recognize the body’s own tissues as harmful. Sometimes, these receptors can also recognize pathogens and cause a cross-reaction with self-antigens. When an infection occurs, it activates these self-reactive cells and creates an inflammatory environment, which can bypass the body’s normal tolerance mechanisms. This combination of genetic predisposition and immune activation from infection can trigger autoimmune diseases.

42
Q

example of molecular mimicry

A

Rheumatic heart disease: T cells that recognize
streptococcal antigens cross react with tissues of the mitral valve of the heart.

43
Q

describe the development of autoimmune disorder

A

1) gentic suscebitiliy
2) faliur of sel tolerance/control
3) infection
4) antigen presenting cells activation
5) recruitment of lymphocytes
6) activation of lymphocytes
7) damage from autoimmune attack
8)autoimmune disease

44
Q
A